Cooperia oncophora

C. oncophora females are about 6–8 mm long, males about 5.5–9 mm.[6] They are light red in color and have a coiled shape. Male worms have a large bursa as shown in Figure 2a. The spicules are 240-300 µm long and have a rounded end and a longitudinal line pattern.[6] L3 stage larvae are hard to differentiate between different species, because they are very similar interspecies-wise. Eggs of C. oncophora however can be easily identified by their parallel walls.

Lifecycle of D. dendriticum

The life cycle of C. oncophora is direct. Free-living L3 stage larvae residing on the pasture are taken up by grazing cattle and pass to the small intestine. Here, they molt to L4 larvae and then to adults. Eggs are passed in the faeces to the pasture. The larvae hatch and grow to L3 stage larvae. Infective L3 stage larvae are then again taken up by grazing cattle and the life cycle repeats. The pre-patent period, which includes the time between infection and egg laying, lasts between two and three weeks. Like other trichostrongylids, early C. oncophora L4 larvae are able to arrest their development under unfavourable environmental conditions such as low temperatures and high dryness, a process termed hypobiosis.[7] L4 larvae can stay arrested up to five months. Arrested development is characterized by a large number of individuals stopping at the same stage of development, a bimodal distribution of worm sizes, and a recent exposure of the host animal to the infectious agent prior to the prepatent period of the infectious agent. During this period of arrested development, the worms stop growing and slow down their metabolism. Arrested development allows the worms to evade many of the anthilmentics commonly used. The recommended doses are based on adult worms and normally developing larvae. Arrested development can be triggered by the following situations: seasonal influences on the larvae while outside the host, the normal host immune response interrupting the normal parasitic phase of the life cycle, or overpopulation of adults that leads to negative feedback preventing the further development of more larvae. It is advantageous for nematodes to enter arrested development as they can survive in hostile environments, cause disease in the host by a large portion of the larvae resuming development, produce large numbers of infectious eggs when the environmental conditions are once again favorable, and avoid susceptibility to various anthilmentics.[8]

Cooperia are considered less pathogenic to livestock than other common gastrointestinal nematode worms: Haemonchus or Ostertagia. However, the pathology caused by Cooperia coupled to its wide range of distribution has huge economic impact to cattle producers.[16][17] Typically calves are affected most adversely. Infection causes appetite reduction and inefficient uptake of necessary nutrients which effects body weight, reproduction and can lead eventually to calf death.[16] Although C. oncophora does not feed on host-blood, it has the capacity to burrow through the gut wall, especially in the proximal location (duodenum) which can lead to anemia[17] in the host.

Ruminants respond to C. oncophora infection using multiple mechanisms, and the degree of response varies based on various host-parasitic factors. Based on the response pattern, a small host proportion is classified as "high responder". These are capable of clearing the parasite rapidly, so that no eggs are detected in the feces, or there is only a very low worm burden after 42 days post infection (p.i.) with 100,000 L3 stage larvae. On the other hand, the "low responder" group is highly susceptible to infection, having a high worm burden and high egg output after 42 days p.i.. Most animals however belong to the intermediate responder group. They react initially similar to the low responder group. Although they can significantly reduce egg output after 35–42 days while worm burden in the intestine remains in range of low to high number.[18]

C. oncophora generally tends to reside in the proximal gut, the first six meters. An effective host immune response subsequently drives the adults towards more distal locations. The fecundity of the parasite decreases in the proximal gut after immune activation, although fecundity in the distal gut remains higher.[18] Antigens of C. oncophora larvae and adult worms are capable of triggering lymphocyte proliferation. Moreover, excretory/secretory products (ES) can pronounce the immune response. Pattern and degree of response varies in primary and secondary exposure.[19] The immune response here is mainly of Th2 type. Primary infection does not involve recruitment of specific lymphocytes to the intestinal mucosa. There are no major changes in the T-lymphocytes subsets of the mesenterial lymph node. Instead γδ-T cells guide the immune proliferation initially after primary exposure. On the other hand, increased B-cell proliferation leads increase in antibodies in serum and mucus secretion.

An experimental infection of calves with 100,000L3 larvae caused gradual increase in adult worm specific IgA and IgG1 continued with increase in IgG1/IgG2 ratio. However, in the mucus, proportion of IgA was higher than IgG1.[18] IgA/antigen complex can bind to the Fc receptor of the eosinophil and thereby induce the release of anti-inflammatory mediators and cytokines which can in turn reduce the worm load. Moreover, it has been demonstrated that secretory IgA (sIgA) in the mucous membrane can activate eosinophils more efficiently than serum IgA.[19]

On the other hand, response to secondary exposure involves increase in CD4+ T-cell in the lymph node, in the peripheral blood and in Payer's patches of the proximal gut. However, CD4+ T-cell numbers decrease in the lamina propria after 28 days of secondary experimental infection. Activated cells from the lamina propria migrate to the lymph node and peripheral blood. Acute inflammation in the primed proximal gut occur earlier and eosinophil level normalizes before 14 days of infection. On the contrary, there is an accumulation of eosinophils in the distal gut at around 14 days while proportion of eosinophil increase again in proximal gut after 28 days. This indicates two waves of eosinophil influx where CD4+ T-cell induces second influx rather first one.[20]

Generally, mast cells are also involved with eosinophils in the protection against nematodes. In case of primary and secondary infections with C. oncophora, no direct involvement mast cells have been proved yet.[19][20]

During secondary infections, even low dose exposure can stimulate immune response at the level of typical high dose exposure. Serum IgE levels are also increased during secondary infections, confirming serological protection. All these events are mast cell independent.[21]

There is a general decrease in the expression of apoproteins after C. oncophora infection. However, the resistant host still maintains higher level of apoproteins compared to low responder. There is a disruption of lipid metabolism.[22][23] It is known that dietary rearrangement of lipid metabolism can give protection against nematode infections. Dietary poly unsaturated fatty acids (PUFA) omega-3 and omega-6 can boost up the protection. Therefore, treatment with omega-3 PUFA has been associated low egg count in the feces.[23] As known from other gut inflammations, over expression of lysozymes (LYZ1, LYZ2, LYZ3) can be observed in the gut after C. oncophora infection. These happens to sustain the inflammatory cascades against parasite antigens. Some other genes encoding cell adhesion molecules including CDH26, collectins and gelectins are up-regulated in infected ruminants.[22] CDH26, eosinophil number recruitment and amount of adult parasites correlates strongly in the mucosa.[24] CDH26 level is positively correlated with Cooperia specific IgA.[25]

Prevention is a difficult task. Cooperia larvae can withstand in adverse environmental conditions and can survive in grass lands even up to a year. Larvae can undergo dormant during winter and can comeback upon suitable conditions. Combined efforts that are taken to prevent typical worm infection are also applicable for Cooperia. These include maintaining a healthy herd, pasture management, careful grazing, plowing the field, avoiding congested and humid environments, keeping calves separately and ensuring hygiene.[17] On the other hand, selective breeding can give rise to "high respondent" or resistant to infection progenies.

Broad spectrum anthelmintics are also effective against adult worms and larvae. There are several benzimidazoles were successful in clearing infection, including albendazole, febantel, fenbendazole, oxfendazole. Moreover, levamisole and several macrocyclic lactones (e.g. abamectin, doramectin, eprinomectin, ivermectin, moxidectin) are reported to be effective. After multiple rounds of exposure adult ruminants can overcome the adverse effects of the parasite however still it act as reservoir for new infection.[17]

The epidemiology of this species can vary by geographic distribution. For example, the northern hemisphere sees arrested development of the L4 stage more often during the winter. The subtropical areas see arrested development more often during the dry seasons. There is not a lot of relevant epidemiology information available. It is known that C. oncophora has been found in temperate climates such as the United States and Brazil. Studies have been done to establish the prevalence in these areas. The lack of information may be due to less frequent reporting of cattle nematodes as compared to the frequency of human nematodes, and that Cooperia oncophora is not commonly reported as the sole cause of infection. C. oncophora often causes secondary infection alongside the infection caused by Ostertagia ostertagi and Haemonchus contortus. O. ostertagi and H. contortus cause more severe signs of infection than C. oncophora. Because of this difference in signs, O. ostertagi and H. contortus are often reported as the cause of disease rather than C. oncophora.[33]